Anthropometric measurements of infants and under five children in Riyadh City

The data presented in this paper are part of the ongoing pediatric nutrition surveillance in ten primary health centers from Riyadh City. A total of 21,507 infants and children under five were included. The mean birth weight was 3027 g, and 8.6% of the children had low birth weights. The measurements showed that there had been no obvious change in the weights and heights of children during the past 13 years. In our results the children classified as moderate and severely underweight were 4.5% and 0.8% respectively. The data showed the average growth of all infants, regardless of feeding pattern, was same or faster than the NCHS reference population, up to approximately six months of age after which their growth became slower than that of the NCHS standards. The prevalence of malnutrition in Saudi Arabia is moderately high, in spite of the high per capita income, and the fact that the government subsidizes locally produced and imported food items. The malnutrition among this age group may be attributed to reproductive or social behavior and genetic factors. The reduction of malnutrition in the last ten years could be largely due to the nutrition and health education programs. There is a need for more comprehensive nutritional health education among the local population.     

Pulmonary hydatidosis--a surgical experience

Twenty-five cases of pulmonary hydatid cysts were studied with emphasis on age, sex and site distribution. In the present study, the youngest patient was of 4 years. Male predominance (2.125:1) with peak incidnce at 21-40 years was observed. Right lung was involved more frequently. Pain chest and haemoptysis were the commonest symptoms. No recurrence and no mortality were reported.     

Clinical and pathologic findings in hereditary spastic paraparesis with spastin mutation

OBJECTIVE: To describe a family with chromosome 2p-linked hereditary spastic paraparesis (HSP) associated with dementia and illustrate the cerebral pathology associated with this disorder. BACKGROUND: HSP comprises a heterogeneous group of inherited disorders in which the main clinical feature is severe, progressive lower limb spasticity. Nongenetic classification relies on characteristics such as mode of inheritance, age at onset, and the presence or absence of additional neurologic features. Several loci have been identified for autosomal dominant pure HSP. The most common form, which links to chromosome 2p (SPG4), has recently been shown to be due to mutations in spastin, the gene encoding a novel AAA-containing protein. RESULTS: The authors report four generations of a British family with autosomal dominant HSP in whom haplotype analysis indicates linkage to chromosome 2p. In addition, a missense mutation has been identified in exon 10 of the spastin gene (A1395G). Dementia was documented clinically in one member of the family, two other affected family members were reported to have had late onset memory loss, and a younger affected individual showed evidence of memory disturbance and learning difficulties. Autopsy of the demented patient confirmed changes in the spinal cord typical of HSP and also demonstrated specific cortical pathology. There was neuronal depletion and tau-immunoreactive neurofibrillary tangles in the hippocampus and tau-immunoreactive balloon cells were seen in the limbic and neocortex. The substantia nigra showed Lewy body formation. The pathologic findings are not typical of known tauopathies. CONCLUSIONS: The authors confirm that chromosome 2p-linked HSP can be associated with dementia and that this phenotype may be associated with a specific and unusual cortical pathology.     

High mobility group proteins 1 and 2 recognize chromium-damaged DNA

Chromium (Cr) is a human carcinogen and a potent DNA damaging agent. Incubation of DNA with CrCl3 resulted in dose-dependent binding of Cr to DNA and, at concentrations >20 microM, altered the electrophoretic mobility of a 100 bp oligonucleotide. We also demonstrate that high mobility group (HMG) proteins 1 and 2 bind Cr-damaged DNA (Cr-DNA). Protein binding was lesion density-dependent, with maximal binding to DNA treated with 100 microM CrCl3. HMG2 binds to Cr-DNA with a calculated Kd of approximately 10(-9) M. These proteins also bound DNA obtained from chromate-treated cells. These results suggest that the covalent attachment of Cr to DNA induces alterations in DNA structure which are recognized by HMG1 and HMG2. Therefore, these proteins may function as Cr-damaged DNA recognition proteins in vivo and as a consequence of binding, may play a role in directing the cellular response to Cr-DNA adduct formation.